Role of iron metabolism and oxidative damage in postmenopausal bone loss

D’Amelio, Patrizia; Cristofaro, Maria Angela; Tamone, Cristina; Morra, Elena; Bella, S. Di; Isaia, Gianluca; Grimaldi, Anastasia; Gennero, Luisa; Gariboldi, A.; Ponzetto, Antonio; Pescarmona, Gianpiero; Isaia, Giovanni Carlo

doi:10.1016/j.bone.2008.08.107

Cited by 60 publications

(40 citation statements)

References 25 publications

(37 reference statements)

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“…Other studies have shown that lipid oxidation caused by excessive levels of ROS may have opposite effects on bone formation [12,25]. Furthermore, an increasing number of studies have provided evidence for a strong relationship between oxidative injury and osteoporosis in diabetes mellitus and at postmenopause [45][46][47]. Thus, the HFD-induced bone loss may also be associated with oxidative stress.…”

Section: Discussionmentioning

confidence: 93%

Expression of Genes Associated with Bone Resorption is Increased and Bone Formation is Decreased in Mice Fed a High‐Fat Diet

Xiao

Cui

et al. 2010

Lipids

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A high-fat diet (HFD) leads to an increased risk of osteoporosis-related fractures, but the molecular mechanisms for its effects on bone metabolism have rarely been addressed. The present study investigated the possible molecular mechanisms for the dyslipidemic HFD-induced bone loss through comparing femoral gene expression profiles in HFD-fed mice versus the normal diet-fed mice during the growth stage. We used Affymetrix 430A Gene Chips to identify the significant changes in expression of the genes involved in bone metabolism, lipid metabolism, and the related signal transduction pathways. Quantitative RT-PCR was carried out on some significant genes for corroboration of the microarray results. At the conclusion of the 12-week feeding, the down-regulation of most of the genes related to bone formation and the up-regulation of most of the genes related to bone resorption were observed in the HFD-fed mice, consistent with the changes in plasma bone metabolic biomarkers. Together, the HFD induced a decrease in the majority of the adipogenesis-, lipid biosynthesis-, and fatty acid oxidation-related gene expression, such as PPARg and APOE. Furthermore, some genes engaged in the related signal transduction pathway were strongly regulated at the transcript level, including IGFBP4, TGFbR1, IL-17a, IL-4, and P53. These results indicate that an HFD may induce inhibitory bone formation and enhanced bone resorption, thus causing adverse bone status.

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Section: Discussionmentioning

confidence: 93%

Expression of Genes Associated with Bone Resorption is Increased and Bone Formation is Decreased in Mice Fed a High‐Fat Diet

Xiao

Cui

et al. 2010

Lipids

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“…1, where the WSassociated clinical features are related to underlying redox anomalies. Each one of the WS-associated clinical complications has well-established aetiological links with oxidative stress as assessed in an overwhelming body of literature (Capell et al 2009;Sendur et al 2009;D'Amelio et al 2008;Herrera et al 2009;Fearon and Faux 2009;Varma and Hegde 2007).…”

Section: The Ws-mitochondria Puzzlementioning

confidence: 99%

Mitochondrial dysfunction in some oxidative stress-related genetic diseases: Ataxia-Telangiectasia, Down Syndrome, Fanconi Anaemia and Werner Syndrome

et al. 2010

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Oxidative stress is a phenotypic hallmark in several genetic disorders characterized by cancer predisposition and/or propensity to premature ageing. Here we review the published evidence for the involvement of oxidative stress in the phenotypes of Ataxia-Telangiectasia (A-T), Down Syndrome (DS), Fanconi Anaemia (FA), and Werner Syndrome (WS), from the viewpoint of mitochondrial dysfunction. Mitochondria are recognized as both the cell compartment where energetic metabolism occurs and as the first and most susceptible target of reactive oxygen species (ROS) formation. Thus, a critical evaluation of the basic mechanisms leading to an in vivo pro-oxidant state relies on elucidating the features of mitochondrial impairment in each disorder. The evidence for different mitochondrial dysfunctions reported in A-T, DS, and FA is reviewed. In the case of WS, clear-cut evidence linking human WS phenotype to mitochondrial abnormalities is lacking so far in the literature. Nevertheless, evidence relating mitochondrial dysfunctions to normal ageing suggests that WS, as a progeroid syndrome, is likely to feature mitochondrial abnormalities. Hence, ad hoc research focused on elucidating the nature of mitochondrial dysfunction in WS pathogenesis is required. Based on the recognized, or reasonably suspected, role of mitochondrial abnormalities in the pathogenesis of these disorders, studies of chemoprevention with mitochondria-targeted supplements are warranted.

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“…Zn stimulates osteoblasts and inhibits osteoclasts [41]. Mg is important in matrix and mineral metabolism in bone [42].…”

Section: Resultsmentioning

confidence: 99%

Rankl Expression and Metabolic Changes in Ovariectomized Rats and the Possible Protection by Vegetable Formula.

Hanafi

2018

Asian J Pharm Clin Res

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Objective: This study was to evaluate complications of osteoporosis in ovariectomized rats and the possibility to ameliorate these changes by consumption of vegetable formula. Furthermore, transcription of mRNA of RANKL gene was matched with bone mass density (BMD) and bone formation marker (human procollagen 1 N terminal peptide [PINP]).Methods: Thirty rats were divided into three groups. The first is non ovariectomized control group (NOVXC), the second is ovariectomized control group (OVXC), and the third is ovariectomized rats supplemented with the vegetable formula (OVXT). Animals were fed for 8 successive weeks. Animals were treated and sacrificed under the recommended ethics of laboratory animal's treatment. The vegetable mixture was formulated with the purpose to correct the bone compromise and supply all the presumed deficient elements and hormone.Results: Chemical analysis showed that the formulated vegetable mixture had a high amount of flavonoids as catechin (100 mg/100 g of dry weight) and polyphenols as tannic acid (1000 mg/100 g dry weight. Furthermore, it had high reducing power (1,1-diphenyl-2-picrylhydrazyl radical showed inhibition percentage of 91.81%.). Several phytochemicals necessary for bone health were demonstrated in the vegetable mixture using highperformance liquid chromatography. RANKL/GAPDH mRNA transcription ratio showed marked an increase in OVXC versus the control NOVXC rats Conclusion:It may be concluded that the plant formula was effective to minimize health hazards in ovariectomized rats and maybe for postmenopause women. Perhaps longer time may be needed for more significant and clear effect.

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Role of iron metabolism and oxidative damage in postmenopausal bone loss

Cited by 60 publications

References 25 publications

Expression of Genes Associated with Bone Resorption is Increased and Bone Formation is Decreased in Mice Fed a High‐Fat Diet

Expression of Genes Associated with Bone Resorption is Increased and Bone Formation is Decreased in Mice Fed a High‐Fat Diet

Mitochondrial dysfunction in some oxidative stress-related genetic diseases: Ataxia-Telangiectasia, Down Syndrome, Fanconi Anaemia and Werner Syndrome

Rankl Expression and Metabolic Changes in Ovariectomized Rats and the Possible Protection by Vegetable Formula.

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